316-Upper Respiratory Disorders

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316-Upper Respiratory Disorders Powered By Docstoc
					Upper Respiratory Disorders
     Debbie King, CFNP, CPNP
            June 2010
 Newborn
   Definition: Infection and/or inflammation of
    conjunctiva in first month of life
   Etiology/Incidence
     Chemical-irritation from silver nitrate or other
      preparations,(occurs in 10%) erythromycin ointment has less
     Gonococcal-perinatal transmission, prophylactic treatment
      with erythromycin ointment 0.5%, topical silver nitrate 1%,
      tetracycline 1%, or povidone-iodine 2.5% (AAP,2003)
     Chlamydia occurs in 50% of newborns with infected mothers
     Other pathogens after one week, include H. flu,
      staphylococcus aureus, group B strep, and HSV
 Signs and Symptoms
   Chemical-mild injection of conjunctiva, presents several hours
    after drop or ointment treatment, last no longer than 3-4 days
   Gonococcal- acute profuse purulent discharge 2-4 days after
    birth with sever lid edema
   Chlamydia- usually presents with mild mucopurulent discharge
    a few days to several weeks after birth, may be recurrent.
    Severe cases may lead to scarring.
   Other bacteria-purulent discharge normally seen on 5th day,
    usually skin contamination or URI
   Virus-serous discharge
 Differential Diagnosis
   Dacryostenosis
   Foreign body
   Corneal abrasion
 Physical Findings
   Chemical-conjunctival hyperemia, minimal lid edema, scanty
   Gonococcal-chemosis, significant lid edema; purulent discharge
   Chlamydia- minimal lid edema, conjunctival hyperemia,
    chemosis, concomitant pneumonia(afebrile, repetitive staccato
    cough, tachypnea and rales)
   Other bacteria-lid edema and purulent discharge
   HSV-possible serous discharge-unilateral injection, mucoid
    discharge, epithelial lesions in cornea, typical herpetic lesions
    may be noted on lid
 Diagnostic test and findings
   Gram and Giemsa stain-gonococci revealed as
    intracellular gram negative diplococci ; chlamydia is
    revealed as basophilic intracytoplasmic inclusions in
    the conjunctival epithelial cells
   Cultures-positive for specific organism
   Direct fluorescent antibody testing for chlamydia
 Management/Treatment
   Chemical-no treatment, resolves spontaneously without
   Gonococcal-hospitalization is necessary, treated with Rocephin,
    topical treatment alone is inadequate and unnecessary when
    systemic therapy is given (AAP,2003)
   Chlamydia conjunctivitis and pneumonia-oral EES QID, for 10
    days, or oral sulfonamides may be used after neonatal period,
    topical not needed and ineffective
   Other bacteria-organism dependent; erythromycin ointment,
    gentamicin gtt , moist compresses
   Stress hand washing, no sharing of towel, ECT.
   HSV- will be treated by ophthalmologists
   Mothers and partners should also be treated appropriately
 Childhood Conjunctivitis
 Definition: Inflammation and/or infection of
  palpebral (lining of eye lids) and bulbar (layer of
  tissue over the sclera) conjunctiva in children one
  month or older
 Etiology/Incidence
   Most frequent ocular disorder in children; may be
    associated with otitis media indication bacterial infection
    with beta-lactamase resistant organism
   Very contagious
   Bacterial is most likely staphylococcus aureus, H Flu, and
    strep pneumoniae
   Viral is most likely due to adenovirus 3,4 or 7. Also caused
    by HSV, or varicella zoster
   Allergic- often with unidentified cause, or seasonal
Childhood Conjunctivitis
 Signs and symptoms
   Pruritus, foreign body sensation, tearing
   Headache
   Possible light sensitivity
   Discharge
     Viral, allergic-watery or thick/stringy mucoid
     Bacterial-purulent
Childhood Conjunctivitis
 Differential diagnosis
   Nasolacrimal duct obstruction
   Blepharitis in older children
   Keratitis ( can be seen with HSV )
   Systemic infection presenting with conjunctivitis, e.g.
    Rubella, Rubeola, Kawasaki
   Periorbital cellulitis
Childhood Conjunctivitis
 Physical findings
   Discharge, rhinitis
   Eyelid edema
   Moderate to severe erythema of conjunctiva; chemosis
   Preauricular adenopathy commonly seen with viral pathogens
   Malaise, pharyngitis and fever may be present
   Cobblestone-like papillary hypertrophy along inner aspect of
    upper lid(vernal conjunctivitis)
Childhood Conjunctivitis
 Diagnostic tests/finding
   Cultures and sensitivities usually unnecessary unless
    Pseudomonas, Neisseria or other virulent organism
   Rule out corneal infiltration (or abrasion) with
    fluorescein stain
  Childhood Conjunctivitis
 Management/Treatment
   Bacterial - respond readily to topical ophthalmic antibiotics e.g.
    Vigamox, ECT. If concomitant otitis media may also treat with
    PO antibiotic
   Viral-artificial tears, steroid gtt by eye DR only
   Herpes-REFER!!!
   Allergic-avoidance of allergens, cold compresses, systemic or
    topical antihistamines, mast cell stabilizers-Zaditor, or Patanol,
    Pataday gtt. Refer if chronic
   Good hand washing, ECT….
   Refer:
      If conjunctivitis is unresponsive to treatment with 2 to 3 days
      If associated with loss of vision, pain, photophobia
      If severe conjunctivitis or with corneal/orbital cellulitis
 Definition: unilateral or bilateral obstruction of the
  nasolacrimal duct, usually at nasal punctal opening
 Etiology/Incidence
   Due to failure of duct canalization during gestation
   May also occur secondary to trauma or infection
   Most common lacrimal disorder in infants
   90% spontaneous resolution by 12 months
 Signs and Symptoms
   Continuous or intermittent tearing with crusting of lashes
 Differential diagnosis
   Conjunctivitis
   Dacryocystitis-inflammation or infection
   Glaucoma
   Intraocular inflammation
   External irritation
 Physical findings
   Tearing
   Expression of thin mucopurulent exudate from
    lacrimal sac
   Inflammation/infection of conjunctiva
   Signs of dacryocysitis-fever,erythema and edema of lid
    and/or over lacrimal sac or duct, excoriation of
    surrounding tissue
 Management/Treatment
   Gently massage lacrimal sac and nasolacrimal duct
   For conjunctivitis or purulent discharge, administration of
    antibiotic gtt
   Referral to ophthalmologist –PRN
   Persistent obstruction and recurrent purulent drainage beyond
    6-12 months may require surgery
   Severe dacryocystitis requires systemic antibiotics and referral
 Definition: obstruction of meibomian glands lining
  posterior margins of upper or lower lids
 Signs and Symptoms
   Progressive swelling of lid
   Slight discomfort (or none at all)
   Minimal redness
 Differential Diagnosis
     Blepharitis
     Hordeolum
     Sebaceous cell carcinoma (rare)
 Physical findings
   Firm, nontender, non movable nodule
   Large chalazion may cause chronic pressure on cornea
    leading to astigmatism
 Diagnostic tests/finding: none indicated
 Management/Treatment
   Small chalazion may resolve without treatment
   Warm compresses
   Treat large, recurrent or infected lesion with antibiotic
    gtt for 7 days
   If unresponsive – refer (may require surgery)
 Definition
   Common acute or chronic inflammation of
    eyelash follicles and meibomian glands of eyelid
   Types
     Seborrheic, ulcerated or combination of both
     Bacterial infection of lash follicles
 Etiology/Incidence
   Seborrheic blepharitis may be associated with
    seborrheic dermatitis, psoriasis, eczema or allergies:
    chemicals, smoke, pollution and cosmetics can
    aggravate condition
   Staphylococcus aureus is primary causative pathogen
   Common in early childhood: associated with down
    syndrome; eczema
 Signs and Symptoms
   Irritation, burning
   Sensation of FB
   Erythema of eyelid margins
   Pruritus
   Loss of eye lashes
 Differential diagnosis
   Chalazion, conjunctivitis, superficial dermatitis
   Hordeolum
   Seborrhea, pediculosis of eyelashes
 Physical findings
   Seborrheic form-hypertrophy and desquamation of epidermis
   Loss of eyelashes
   Translucent, easily removed scales
   Ulcerative form-purulent inflammation with ulcer formation
    on lids with erythema and bleeding
 Diagnostic tests/finding: none indicated
 Management/ Treatment: similar for both types
   Warm moist compresses
   Daily mechanical scrubbing and cleansing of lid margins with
    cotton swab, dipped in dilute baby shampoo
   Topical antibiotic gtt
   May need to use shampoo with selenium sulfide
   Recurrences are common
Orbital/Periorbital Cellulitis
       Orbital-inflammation of the orbital contents
 posterior to orbital septum
       Periorbital-inflammation/infection of the skin and
 subcutaneous tissue surrounding eye; often associated
 with trauma, septicemia, sinusitis and bacteremia or
 local infection near the eye
Orbital/Periorbital Cellulitis
 Etiology/Incidence
   Orbit or preseptal areas are infected from local trauma
    or spread from proximate structures
   Most common causes of bacterial orbital cellulitis in
    children are paranasal sinusitis and ethmoiditis
   Other causes include stings or bites, impetigo, or FB
   Most common organisms are Staph, Strep, H. flu
   Periorbital cellulitis much more common than orbital
Orbital/Periorbital Cellulitis
 Signs and Symptoms
   Orbital
      Insidious onset
      Orbital pain, headache
      Fever
      Potentially devastating consequences
  Periorbital
    Acute onset of unilateral eyelid swelling
    Warmth, swelling and tenderness of skin
    Eye itself and vision are usually normal
  Both
    Rhinorrhea, fever (102+)
Orbital/Periorbital Cellulitis
 Differential Diagnosis
   Differentiate between orbital (within true Orbit),
    periorbital or preseptal cellulitis
   Edema secondary to trauma
   Allergic periorbital edema
   Insect bite
Orbital/Periorbital Cellulitis
 Physical findings
   Orbital cellulitis
     Lid edema
     Chemosis
     Proptosis
     Deceased ocular mobility
     Decreased visual acuity
     Ophthalmoplegia(paralysis of eye muscles) and
      Proptosis(protrusion of eyeball)-classing findings and
      distinguish orbital from periorbital
Orbital/Periorbital Cellulitis
  Periorbital
    Unilateral eyelid edema
    Erythema
    Tenderness of overlying skin
    Visual acuity usually normal
Orbital/Periorbital Cellulitis
 Diagnostic Tests/findings
   Visual acuity-decreased with orbital only
   Sinus roentgenograms or CT scan –determine sinus
   Orbital sonography-determine orbit involvement
   CBC with diff- leukocytosis
   Blood and/or eye cultures-determine pathogen
   Lumbar punctures with infants-rule out sepsis
Orbital/Periorbital Cellulitis
 Management/Treatments
   Prompt assessment, treatment and referral!!
   Systemic antibiotic therapy, IV or IM
   Moderate to severe cases or under 1 year may need
   Complications may include loss of vision, abscess,
    meningitis, thrombosis in the retina or sinus
   Hib vaccine brought sharp decline in annual rate!
 Definition: ocular misalignment
   Exotropia-eyes deviate outward
   Esotropia-eyes deviate inward
   Hypotropia-downward
   Hypertropia-upward
 Etiology/Incidence
   Constant strabismus is –tropia
   Intermittent alternating esotropia or exotropia is
    normal the first 6 months of life
   Historical risk factors-prematurity, family hx, CP,
    chromosomal and genetic anomalies, prenatal drug
    exposure, head trauma, and any ocular defects
 Suppression is an adaptation to diplopia-without correction
  permanent loss of vision is probable
 Acquired strabismus occurring after 6 months is usually from
  cataracts, retinoblastoma, or high refractive errors
 Occurs in 4% of children under 6 years; esotropia is most
 Patients with congenital vision loss are more likely to develop
  esotropia; and with acquired vision loss are more likely to develop
 Pseudostrabismus-eyes appear to be crossed due to epicanthal
  folds on either side of bridge of nose; no real ocular deviation
 Signs and Symptoms
   Varies with age
   Squinting
   Decreased vision
   School problems
   Head tilting
   Face turning
   Over pointing
   Awkwardness
 Differential diagnosis
   Cataracts
   Retinoblastoma
   Anisometropia
   High refractive errors
   Amblyopia
   Head trauma
   Other congenital eye muscle syndromes
 Physical findings
   Misalignment of eye(s)
   Intermittent, alternating or continuous esotropia,
    exotropia, hypertropia or hypotropia
 Diagnostic tests/finding
   Abnormal Hirschberg (corneal light reflex unequal)
    and/or cover/uncover test
   Vision screen-may reveal refractive errors
 Management/Treatment- referral con’t
   Establish period of onset, progression, frequency and
    amplitude, family Hx, evidence of any associated
    neurological or other disorders
   Refer-
       Over 6 months with intermittent or fixed
       Fixed off set
       With other deviations from normal
       Signs of differential diagnosis present
       Immediate if hypotropia or hypertropia is present –any age
Management/treatment con’t
      Acquired-appropriate treatment depending on
 pathology and/or refractive errors
      Patching of fixing eye forces use of deviating eye,
 eye exercises, corrective lens as needed, surgical
 alignment may be considered
 Definition; involuntary, horizontal, vertical, rotary, or
  mixed rhythmic movement of eyes
 Etiology/Incidence
   Caused by either fixation, conjugate gaze, or vestibular
   May be familial
   Associated with albinism, refractive errors, CNS abnormalities,
    diseases of inner ear and retina
   Classified according to direction of movement
 Signs and symptoms
   Irregular eye movements
   Abnormal head movements; may be rhythmic
 Differential diagnosis; underlying cause
 Physical findings
   Involuntary rhythmic eye movements
   Vision screen may be abnormal
Diagnostic tests/finding
 abnormal visual acuity test
 will need CT- will be ordered by specialist
 refer to ophthalmologist and neurologist
 treat underlying cause (Tumor until proven otherwise)
 Monitor closely
External Otitis (Otitis Externa)
 Definition: acute infection and/or inflammation of
  external auditory canal: swimmers ear
 Etiology/Incidence
   More common in summer
   Common organisms are pseudomonas, staphylococcus aureus,
    strep pyogenes, Enterobacter, proteus, klebsiella, staph
    epidermis, and fungi
   Loss of protective cerumen or chronic irritation
   Trauma disrupting lining e.g. FB, digital irritation
   Excessive dryness (dermatitis, hair spray)
External Otitis (OE)
 Signs and symptoms
   Itching (early)
   Acute and possibly severe pain with manipulation of
    pinna/tragus, or mastoid pain
   Pressure/fullness in ear, possible hearing loss
 Differential diagnosis
   Acute otitis media with perf
   Dental infection, mastoiditis
   FB
   Eczema
External Otitis
 Physical findings
   May be difficult to see TM which is usually normal
   Edematous/erythematous external canal
   Black spots on TM indicate fungus
   Furuncle may be noted
   Otorrhea, occasional lymphadenopathy
   Observe for signs of mastoiditis or cellulitis beyond
    the external canal
External Otitis
 Diagnostic tests/findings
   Culture of discharge unneeded unless unresponsive to
   Referral with severe mastoid pain
 Rechecks to be scheduled PRN
   Education is very important
   Patient and parents must watch for increased
  External Otitis
 Management/Treatment
   Withdraw any FB or debris
   Topical antibiotic gtt that contain a corticosteroids for 7 days
      Children with ear tubes can get OE secondary to the drainage from OM and use
       the same meeds
         Ciprodex, Cortisporin, Floxin
   Wick-PRN
   For a severe case use PO antibiotics with good skin coverage
      Augmentin, Ceftin, Omnicef, Keflex
   Pain med-PRN
   Re-examine PRN
   Prevention- ‘swim ear’ drops, blow dry
   I and D of furuncle-PRN
   Fungal infection-teat with antifungal
Acute Otitis Media
 Definition: inflammation of the middle ear with fluid/pus or
  with otorrhea (discharge/pus from the ear through a
  perforation and associated signs and symptoms of ear
   Otalgia
   Fever
   Irritability
   Anorexia
   Vomiting
Acute Otitis Media
 Etiology/Incidence
   Fluid/pathogen accumulation in middle ear to Eustachian tube
    malfunction secondary to obstruction caused by allergies, viral
    infections, decreased patency and/or other mechanical factors
 Diagnosis requires
   History of acute onset with signs and symptoms
   Presence of middle ear effusion
     Bulging, decreased mobility, air fluid level, otorrhea-pus
   Signs and symptoms of middle ear inflammation
Acute Otitis Media
 Common pathogenic agents
   Streptococcus pneumoniae #1
   Haemophilus influenzae 25-30%
   Moraxella catarrhalis 10-20%
   Others include staphylococcus aureus, GABHS and
    pseudomonas-more common with chronic OM
   Viruses-influenza, RSV,adenovirus,parainfluenza,coronavirus
   Prevalence of Beta-lactamase producing strains highest in past
    15 years
   Increase in drug resistant bacteria
   No growth found in at least 16% of AOM
 Acute Otitis Media
 Predisposing factors
   Physiological- size of people under 6 years
   Hereditary
   Common with URI
   Bottle feeding in supine position
   Craniofacial abnormalities
   Allergic rhinitis
   Smoke!
   Day care!
   If develop early are prone to recurrent OM
   Natural history of untreated OM-70-90% resolve untreated
Acute Otitis Media
 Signs and Symptoms
     Fever possible
     Complaints of fullness or pain
     Poor appetite/feeding
     Sleep disturbance
     Irritable
     Nausea/vomiting
     Runny nose
     Tugging on ears
Acute Otitis Media
 Differential diagnosis
   Crying child with normal red TM’s
   Damage to TM
   Otitis media with effusion (fluid not infection)
   Tympanosclerosis
   Cholesteatoma
   Otitis externa
   Rare complications-mastoiditis; sepsis, hearing loss,
    developmental/speech delay
Acute Otitis Media
 Physical Findings; diagnosis is determined by changes in
  color, contour, vascularity, and mobility of the TM
   Color is erythematous or yellow or opaque
   Contour may be dull or bulging; light reflexes usually distorted
    or absent other landmarks absent
   Distinct vascularity
   May be bulging or not
   Mobility decreased or absent
   May have a bullae on the eardrum
   Conductive hearing loss
Acute Otitis Media
 Diagnostic tests/Findings
   Pneumatic otoscopy-visualize
   Tympanometry
   Hearing tests
   Language screen
       Acute Otitis Media
 Management and Treatment
   Judicious use of antimicrobials, consider no treatment 1-3 days, if no
    better start med for children 2 and older
        Amoxil, Augmentin, Omnicef (book says Rocephin 3rd) then Rocephin
        If vomiting Rocephin first line for one day then PO
        If PEN allergic use cephalosporin –Ceftin, Omnicef
      Select appropriate antibiotic
      Maintain realistic expectations
      Tympanocentesis-rarely done
      Monitor residual OME 6-8 weeks
        If lasts longer than 4 months refer
    Pain management PO or gtt
    Refer- PRN
    Great algorithm for treatment in text
   Complications of AOM
 Tympanosclerosis
   White plaque like appearance-granulation tissue
     Continued inflammation can cause adhesion and may form a
   Cholesteatoma
       Addressed later in the lecture
   Complications of AOM
 Tympanic Membrane Perforation
   May be caused by full TM that ruptures
   May be left after tube removal
   Usually heals in two weeks
   If persistent beyond 6 months may need repair
   Precautions
     No diving
     May use plugs
Complications of AOM
 Facial Nerve Paralysis
   Facial nerve crosses the middle ear
   Nerve may be incompletely encased in bone
     With inflammation during OM- may cause acute facial nerve paralysis
     With paralysis and middle ear fluid refer for possible myringotomy and
   Chronic Suppurative Otitis Media
     Persistent otorrhea with tubes or perforations
     May be signs of a cholesteatoma
     Refer to ENT for suction, culture and treatment
Recent Study
 January 28, 2010 — The management of acute otitis media
  (AOM) without antibiotics has not increased after publication
  of the 2004 American Academy of Pediatrics (AAP) and the
  American Academy of Family Physicians (AAFP) clinical
  practice guideline on AOM allowing "watchful waiting,"
  according to the results of a study reported Online First
  January 25 and to be published in the February issue of
Otitis Media with Effusion
 Definition; Inflammation/fluid accumulation in middle ear
  with decreased TM mobility but without signs and symptoms
  of infections, also called serous, secretory, mucoid, and
  allergic otitis media or glue ear
Otitis Media with Effusion
 Etiology/Incidence
   Caused by Eustachian tube malfunction as frequent sequelae of
   OME account for 25-35% of all cases of OM
   30-40% have OME with allergic rhinitis
   Majority clear within 2-3months
   Mild to moderate hearing loss with possible language delays or
    behavioral difficulties may be seen
Otitis Media with Effusion
 Signs and Symptoms
   Sometimes none or mild discomfort
   Behavioral changes (hearing loss)
   Talking loud
 Differential diagnosis
   Same as AOM
Otitis Media with Effusion
 Physical Findings
     Color-opaque or translucent, may see fluid levels or bubbles
     Contour-appears retracted due to negative pressure
     Vascularity-none seen
     Mobility-decreased, tympanometry reveals high negative
 Diagnostic tests; same as AOM
Otitis Media with Effusion
 Management/Treatment
   Most cases resolve without antibiotics
   Limit use of antibiotic prophylaxis
   Steroids, oral and nasal limited value, per new research
   Limit passive smoke exposure
   Treat other infections (sinusitis)
   Control allergies
   Consider surgery for chronic OME
   Decongestants and antihistamines not helpful
   Follow up 4 weeks or PRN
Tympanostomy Tubes
 Procedure
   Surgical incision of ear drum (myringotomy with
    placement of ventilation tube) to relieve pressure and
    drain pus and fluid from middle ear
   Two types
     Short term lasts 8-15months
     Long term lasts > 15 months
Tympanostomy Tubes
 Etiology/Incidence
   One million tubes inserted annually
   Indicated for children with failed antibiotic treatment
    with multiple meds, or with frequent recurrent
    episodes, or with hearing loss longer than 2-4 months
   Increased number of resistant bacteria, possibility of
    more frequent use of tubes
Tympanostomy Tubes
 Management/Treatment
   Fitted ear plugs????
   If drainage occurs form tubes, treat with antibiotic otic
   gtt (Cipro HC, Cortisporin, Floxin)
Other Ear Issues
 Foreign Body
   Addressed later in the lecture
 Hematoma of the Pinna
   Trauma
   Appears as a boggy purple swelling of the upper half of the ear
   If not treated, can cause pressure necrosis and lead to cauliflower ear
      Refer
 Congenital ear malformation
   Lop ears-folded down-surgical correct
   Low set associated with renal malformation
   Preauricular tags, pits
     If pits become infected treat with antibiotic and refer to ENT for repair
 Definition-infection of the mastoid antrum and air cells
  with potential destruction of the mastoid airspaces, a
  suppurative complication of OM
 Etiology/Incidence
     Uncommon, due to successful treatment of OM
     Develops secondary to OM
     Unusual before 2 years of age
     Common pathogens- strep pneumoniae ,strep pyogenes,
      staphylococcus aureus; less common- Hflu; rare pseudomonas,
      mycobacterium tuberculosis, Mcat
 Signs and symptoms
   Pain, swelling and tenderness behind the ear
   Fever or irritability
 Differentials
        Extradural abscess
        Subdural empyema
        Focal otic encephalitis
 Physical findings
   Severe tenderness over mastoid bone
   Mastoid area often edematous with erythema
   Presence of AOM or OE
   Pinna displaced downward and outward (late)
   Narrowing of ear canal due to pressure from mastoid
   Purulent drainage
 Diagnostic tests/finding
   CBC-elevated WBC
   Blood culture-rule out sepsis
   PDD-rule out exposure to tuberculosis
   X-ray or CT scan of mastoid
   Tympanocentesis-identify pathogen
   Lumbar puncture-rule out meningitis
 Management/Treatment
   Prompt referral to ENT / hospital
   Incision and drainage of abscess
   IV antibiotics
   Complications-meningitis, brain abscess, cavernous
    sinus thrombosis, acute suppurative labyrinthitis, facial
   Oral systemic antibiotic for 4-6 weeks after discharge
   Do Not Miss It!
 Definition: cyst like mass with lining of stratified
  squamous epithelium filled with desquamated debris;
  most common in middle ear and mastoid are
 Etiology/Incidence
   Congenital or acquired
   varied theories; inflammatory process; perforation or
    failure of desquamated tissue to clear
   Incidence unknown
   If surgery delayed, can invade and destroy temporal
    bone then to brain
   If untreated may lead to facial nerve paralysis,
    intracranial infection
 Signs and Symptoms
   Dizziness
   Hearing loss
   May have no symptoms
   May have OM symptoms
 Differentials
   Aural polyps
 Physical findings
   Pearly white, shiny, greasy lesion on or behind
    tympanic membrane
   History of chronic OM with foul smelling purulent
 Diagnostic test/finding
   Audiogram to rule out hearing deficit
 Management/ Treatment
   Referral to ENT for surgical excision
   Complications
     Irreversible structural damage
     Permanent bone damage
     Facial nerve palsy
     Hearing loss
     Intracranial infection
Allergic Rhinitis
 Definition; IgE mediated response to inhaled allergens or
  irritants producing nasal mucosa inflammation
 Etiology/Incidence
    Types-seasonal or perennial depending on
     exposure/sensitization to allergen
     Seasonal- inhaled pollens
     Perennial- house dust mites, mold spores, animal dander
      (rare under 2 years)
Allergic Rhinitis
 Etiology con’t
   Most common pediatric atopic disease, commonly
    associated with conjunctivitis, sinusitis, OME and/or
    atopic dermatitis
   Strong genetic predisposition
Allergic Rhinitis
 Signs and Symptoms
   Chronic, clear nasal discharge
   Episodes of sneezing with itching of eyes, ears, nose,
    palate, pharynx
   Open mouth facies, snoring with sleep
   Excessive tearing
   Purulent secretion may indicate secondary infection
   Symptoms year-round with perennial rhinitis
Allergic Rhinitis
 Differential diagnosis
   Bacterial or viral upper respiratory infection
   Vasomotor rhinitis
   Congenital or anatomical abnormalities leading obstruction
 Physical findings
   Allergic shiners, and salute with nasal crease
   Hypertrophied turbinates; halitosis
   Nasal mucosa pale bleu, boggy, and edematous with watery or
    mucoid secretions
Allergic Rhinitis
 Diagnostic tests/findings
   Nasal smear for eosinophls-10% is confirmatory
   RAST and skin testing-elevations or reactions to specific
 Management/ treatments
   Identify and avoid allergens
   Environmental controls-no carpet,drapes,stuffed animals.
    Covers for mattress and pillows, decrease humidity, use air
    purifiers, avoid smoke
   Drug TX- combo antihistamine, nasal steroid, Singulair
   Referral if symptoms not responsive
Chronic Rhinitis
 Definition; Chronic nasal discharge with or without acute
 Etiology/Incidence
   May reflect underlying disorder e.g., nasal polyps, chronic
    sinusitis, chronically infected tonsils, CF, allergy, FB, deviated
    septum, congenital malformation, syphilis
   May result from prolonged topical nasal decongestant use
Chronic Rhinitis
 Signs and Symptoms; variable
   Foul smelling, nasal discharge
   Possible bloody discharge; FB, syphilis
   Disturbances in taste and smell
   Fever with superimposed infection
 Differentials
   Allergic rhinitis
   Sinusitis
   FB
   URI
   Chronic Rhinitis
 Physical findings;
   Excoriation of anterior nares and upper lip
   Nasal discharge- usually clear
         FYI- color of mucus does not matter in children

 Management/ Treatment-directed at underlying
   Antibiotic for bacterial infection
   Environmental controls
   Special attention to nutritional status, rest and prevention
    of exposure to new infections
Nasal FB              FYI
 May be food, toys, erasers, beads, bugs, stones, batteries
 Initial sx include sneezing, rarely pain, may lead to
 Physical finding is unilateral foul smelling nasal discharge
  and/or visualization of FB
 Remove or refer and treat infection if present
 Reassure parents this very common
Epistaxis            FYI
 Most cases are benign and frequent
 Originates in from the anterior portion of the nasal
    septum called the Kiesselbach area
   Usually caused by trauma, picking, or dry air, and rarely
    by infection or FB
   Chronic and heavy bleeds need clotting workup to rule
    out hemophilia, anemia, leukemia, ITP, or platelet
   Rare, rare- is hypertension, or CF
   Treat- saline spray and antibiotic ointment to nares
Oral candidiasis FYI
 Common yeast infection or oral cavity
 Most common in infants, can also be in older children
  following steroids, antibiotics, or with weak immune
 White patches that do not wipe away indicate make
 Treat with antifungals and good cleaning practices
 Cases seen in non-infants with out risk factors indicates a
  workup for HIV/ DM
Aphthous Ulcers                    FYI
 Shallow painful mouth ulceration
 Caused by trauma, stress, sun, allergies, endocrine, or
  hematological disorders
 Differentials-herpetic lesion, herpangina (coxsackievirus A),
  trauma, burns, hand-foot-mouth (coxsackievirus
 Treat with pain meds, or rinses
 Periodic fever, aphthous stomatitis, pharyngitis and adenitis (PFAPA)
  syndrome is a medical condition, typically starting in young children, in which
  high fever occurs periodically at intervals of about 3-5 weeks, frequently
  accompanied by aphthous ulcers, pharyngitis and/or adenitis. The syndrome
  was described in 1987 and named two years later. The key symptoms of PFAPA
  are those in its name: periodic high fever at intervals of about 3-5 weeks, as well
  as aphthous ulcers, pharyngitis and/or adenitis. In between episodes, and even
  during the episodes, the children appear healthy. At least 6 months of episodes.
  Recurrent negative throat cultures. Other causes excluded (EBV, CMV). PFAPA
  is frequently discussed together with other periodic fever syndromes, but it is
  unknown whether the cause is primarily genetic or due to an initial infection. A
  possible treatment for PFAPA is a single dose of prednisone (1-2 mg per kg
  body mass) at the beginning of each fever episode.
Pharyngitis and Tonsillitis
 Definition; acute inflammation and infection of the
  throat; when tonsils are main focus of inflammation,
  tonsillitis is more appropriate term
 Etiology/Incidence
   Causes vary by geographic location, season, age, and
    amount/time of exposure, most common in 4-15 year
Pharyngitis and Tonsillitis
 Eti/inc cont
   Viruses
     Virus is most probable cause, with congestion
     Adenovirus (12 types) account for 23%
     EBV
     Influenza A,B, RSV, Parainfluenza, CMV, Rotavirus
     Enterovirus(coxsackievirus A and echovirus) seen in
      the summer and fall
Pharyngitis and Tonsillitis
 Et/in con’t
   Bacterial
     GABHS- 10-15%, typically in winter and spring
     Hflu-less common now with HIB vaccine
     GC- ask if sexually active -if indicated
   Other causes
     Mycoplasma pneumoniae-5% school age children
     Fungal
     Parasites
     Streptococcal toxin postulated as cause of Kawasaki
Pharyngitis and Tonsillitis
 Con’t
   Noninfectious causes (50%)
     Trauma from smoke, heat, alcohol
     Allergic rhinitis or PND

   Transmission-through exposure to infected respiratory
   secretion, shared food or drinks and rarely pets
Pharyngitis and Tonsillitis
  Complications
    Peritonsillar or retropharyngeal abscess or cellulitis
    Cervical adenitis, AOM, sinusitis, pneumonia
    Acute rheumatic fever in untreated GABHS, can be
     prevented if treated within 9-10 days of initial complaints of
     sore throat
    Glomerulonephritis-host/immune response to nonrenal
     infection with GABHS, not all strains are nephritogenic,
     manifests in 1-3 weeks after pharyngeal or sinus infection of
     GABHS, unrelated to treatment
Pharyngitis and Tonsillitis
 Signs and Symptoms; common symptomatology with
 some variability by causative organism
   Sudden or gradual onset of symptoms
   Sore throat
   Fever, variable
   Headache, anorexia, occasional nausea, abdominal pain and
   Viral pharyngitis- hoarseness, conjunctivas, runny nose, cough,
    cold symptoms
   GABHS- usually seen over 2 years, sudden onset of fever, HA,
    abdomen pain, vomiting, rash, strawberry tongue may be
Pharyngitis and Tonsillitis
 Differentials
   Stomatitis
   Peritonsillar or retropharyngeal abscess
   Epiglottitis
   Allergic rhinitis, postnasal drainage
Pharyngitis and Tonsillitis
 Physical Findings
   Erythema of pharynx, petechial lesions with or without ulcers,
    petechial lesions on uvula and soft palate common with GABHS
   Enlarged tonsils with exudate (1/3-GABHS)
   Erythema of nasal mucosa with coryza
   Cervical nodes usually enlarge with possible tenderness
Pharyngitis and Tonsillitis
 Diagnostic Tests/Findings
   Rapid strep test to determine GABHS
     70-85% sensitivity, 95% specificity
     Treat if positive, throat culture to confirm negative
   CBC-WBC elevated with bacterial infection;
    decreased with viral agent
   Consider other studies, dependent on history , age,
    and clinical presentation; mono spot, EBV titers,
    culture of GC and rarely- for diphtheria
Pharyngitis and Tonsillitis
 Management/Treatment
   Viral- supportive care
     Saline gargles, lozenges, Benadryl and Mylanta
     Analgesic for fever and pain
     Encourage fluids
   Bacterial
     GABHS-Amoxil, PENVK, Bicillin, Keflex, ECT.
      Communicability is eliminated after 24 hours of TX
     GC-one IM injection of Ceftriaxone
     Diphtheria-hospital
     Mycoplasma EES
Pandas FYI
 http://circ.ahajournals.org/cgi/reprint/CIRCULATIONA

 Various thoughts on the validity of the diagnosis and the
  appropriate treatments
Acute Nasopharyngitis
common cold
 Definition; acute viral infection of upper respiratory
  tract with potential involvement of nasal passages,
  sinuses, Eustachian tubes, middle ears, conjunctiva and
Acute Nasopharyngitis
 Etiology/Incidence
   Causative pathogens
      Over 100 infectious pathogens-RSV most common
      Other common pathogens include parainfluenza viruses, corona
        viruses, adenoviruses, enterovirus, influenza viruses, mycoplasma
   Pathogen shed in large amounts through nasal secretions and easily
    spread through self-inoculation from fingers to hands to objects
   Universal susceptibility ; children average 5-8 infections / year with a
    peak incidence during first 2 years
   Increased susceptibility associated with active/passive smokers
   More frequent in crowed situations (daycare)
   Occurrence in cooler months in temperate climates-peaks in early
    fall, late Jan and early April
Acute Nasopharyngitis
 Signs and symptoms
   Infants
    Irritability, restlessness, fever
    Rhinorrhea
    Occasional diarrhea
    Changes in feeding and sleep patterns
  Older children
    Afebrile or low grade fever, stuffy nose, water discharge
    Sore throat, sneezing, cough, chills
    Occasional headache, malaise
Acute Nasopharyngitis
 Differentials
   Underlying secondary bacterial infections
   Allergic rhinitis
   FB
   Substance abuse in older patients
   Over use of medicated nasal sprays
Acute Nasopharyngitis
 Physical findings
   Coryza
   Inflamed, moist nasal mucosa and oropharynx
   Chest is clear
 Diagnostic tests/findings
   Viral cultures- expensive, usually not necessary
   If suspicious of differential DX, consider strep test, nose
    culture, drug screen, sinus series
Acute Nasopharyngitis
 Management/Treatment
   Analgesics for sore throat, muscle aches, ECT
   Relief of nasal congestion
     Saline gtt, gentle aspiration-rarely done is best
     Cool mist, one night, or few hours daily for few days
     Antibiotics, antihistamines and decongestants not
      recommended in young children and infants
     Older children may trial symptomatic relief-less is
Acute Nasopharyngitis
 Management cont
   If symptoms persistent beyond 10-14 days, consider
    secondary infection
   Maintain hydration, also helps to liquefy secretions
   Prevention
     Good hygiene
     Limited exposure to crowds
Retropharyngeal Abscess
 Definition; Inflammation of posterior aspect of pharynx
  with suppurative retropharyngeal lymph nodes
   The retropharyngeal nodes drain the adenoids, nasopharynx and
    paranasal sinuses
 Etiology
   Causative pathogens-GABHS-most common, anaerobic
    organisms, staph aureus
   In older children- usually superinfection from penetrating
    injury to posterior wall of oropharynx
   Relatively rare infection; most common in children 2 and under
    but seen in children up to 4 years.
Retropharyngeal Abscess
 Signs and Symptoms
  Acute onset of high fever with persistent throat
  Drooling due to difficulty in swallowing
  Tachypnea, dyspnea, stridor
  Neck and head hyperextension (holds her/his
   head/neck in one position usually against
   parents shoulder)
Retropharyngeal Abscess
 Differentials
   Epiglottitis
   Peritonsillar abscess
   Laryngotracheobronchitis (croup)
   Acute mono
   Acute pharyngitis
   Bacterial tracheitis
   Meningitis
Retropharyngeal Abscess
 Physical findings
   Toxic appearing child neck and head in hyperextension
   Noisy, gurgling respiration
   Drooling
   Stridor, airway obstruction
   Prominent swelling over one side posterior pharyngeal
    wall- confirms DX
Retropharyngeal Abscess
 Diagnostic tests/findings
   Lateral neck X-ray- retropharyngeal space wider than C4
    vertebral body
   CBC-elevated WBC\CT to visualize abscess
 Management/Treatment
   IMMEDIATE and EMERGENCY referral to ENT
   Hospitalization necessary
      ICU care needed to keep airway open
      Surgical incision and drainage
      IV antibiotics-PCN, clindamycin
Peritonsillar Abscess
 Definition; infection of tonsils spreading to tonsillar fossa
  and surrounding tissues (peritonsillar cellulitis) if left
  untreated, tonsillar abscess forms
   Pain begins before physical findings
 Etiology/Incidence
   GABHS-most common
   Staph aureus, anaerobic microorganisms
   Can occur at any age, more common in older
   Complication of untreated peritonsillar abscess-lateral
    pharyngeal abscess leading to possible airway obstruction;
    aggressive early treatment will prevent suppuration
Peritonsillar Abscess
 Signs and Symptoms
   Severe sore throat with high fever
   Toxic appearance, muffled voice, spasms of jaw
   Difficulty swallowing and drooling in severe cases
   Bad breath
 Differentials
   Retropharyngeal abscess
   Epiglottitis
Peritonsillar Abscess
 Physical Findings
   Unilateral enlargement of tonsil, bulging medially with
    anterior pillar prominence!!
   Soft palate and uvula edematous, erythematous, uvula
    displaced toward unaffected side!
   Extreme tonsillar tenderness on palpation
 Diagnostic tests/findings
   CBC-WBC increased
   Rule out GABHS (but could have strep and Abscess)
Peritonsillar Abscess
 Management/treatment
   Surgical incision and drainage often necessary
   Possible need for hospitalization
   Antibiotics-PNC-IM or IV or PO
   If not hospitalized, daily follow up indicated until stable
 Ludwig Angina
   Rapidly progressive cellulitis of submandibular space, causing airway
    obstruction and death
   Submandibular space extends from the mucous membrane of the floor
    of the mouth to the musculare and facial attachments of the hyoid
   Is encountered infrequently in infants and children
   Initiating factor is dental disease is over 50% of cases
   May have a history of injury to floor of the mouth
   Group A strep is usual cause
   Will have fever, tender swelling of the floor of the mouth with tongue
    enlargement which is painful
   Can lead to airway obstruction
   Treat with high dose IV clindamycin pending cultures
Cervical Lymphadenitis
 Definition; inflammation affecting one or more
  cervical lymph nodes
 Etiology/Incidence
   Pathogens-
     GABHS is cause in 70%
     Strep pyogenes, staph aureus-more often need surgery
     Mycobacterium tuberculosis
     Other organisms e.g. viral, fungal, parasitic
   Secondary to local infection of ear, nose, or throat
   Prevalent among preschool children
Cervical Lymphadenitis
 Signs and Symptoms
   Complaints of swollen neck or face
   Fever
   Stridor, hoarseness, drooling if adenopathy impinges on airway
 Differentials
   Bilateral cervical adenitis-mono, tularemia, diphtheria
   Sub acute or chronic adenitis-cat scratch, viral
   Atypical mycobacterium-tuberculosis
   Cervical node tumors e.g. leukemia, neurofibromatosis
   Mumps, cyst, hematoma
Cervical Lymphadenitis
 Physical Findings
   Large unilateral cervical mass, greater than 2-6 cm
   Erythema may be present
   Extreme tenderness on palpation
     Except with cat scratch may only be mildly tender
Cervical Lymphadenitis
 Diagnostic Tests/Findings
   CBC-moderate to marked WBC
   Mantoux test –R/O TB
   EBV titers
   Throat culture- R/O GABHS
   Serology tests if not resolving (EBV, Toxoplasmosis,
    CMV, Histoplasmosis)
   Aspiration of node if fluctuant-aerobic/anaerobic
     IF the cause is TB the node needs to be fully removed to
      avoid a draining sinus tract
Cervical Lymphadenitis
 Management/Treatment
   With no evidence of sepsis treat empirically with oral antibiotic,
    Augmentin , Keflex for 10 days
   Measure and follow size of node
   Pain med PRN
   Re-evaluate frequently, with no improvement may need
    admission for IV meds
   Referral to ENT if not improving
   Surgery may be necessary
   Persistent unexplained, symptomatic node, increasing in size
    despite treatment, refer for biopsy

 Definition; severe, rapidly developing inflammation and
  swelling of the supraglottic structures leading to life
  threatening upper airway obstruction
 Etiology/Incidence
   Pathogens-GABHS,pneumococci,Hflu
   Can occur any age, mostly 2-7 years
   Decreasing incidence with HIB vaccine by 99% with vaccinated
 Signs and Symptoms
   Acute, sudden onset of high fever, severe sore throat, muffled
    voice, drooling, poor color, labored breathing in a previously
    well child
   Choking sensation, refuses to speak
   Restless, irritable, anxious, apprehensive, frightened
   Hyperextension of neck, leaning forward and chin thrust out,
    prostration; sniffing dog, or tripod position, provides best
    possible airway
 Differentials
   Acute laryngeal edema, croup syndrome, FB
   Pertussis, diphtheria, Kawasaki
   Bacterial tracheitis, retropharyngeal abscess
 Physical findings
   Rapidly progressive respiratory distress
   Toxic, distressed appearance
   Beefy erythematous epiglottis
   If epiglottitis suspected, do not attempt to visualize
 Diagnostic tests/finding
   CBC-WBC greater than18,800-low priority test
   Cultures of blood, tracheal or epiglottis secretions-50% of
    cases, positive for Hflu type b
   Radiograph-lateral neck shows a thickened/swollen epiglottis
    (thumb sign) may elect not to perform radiograph due to
    possibility of airway obstruction and respiratory arrest; airway
    can be safely visualized in surgery
 Management/treatment
   Requires prompt recognition and treatment; Represents a true
    EMERGENCY; death can occur in hours
   Provide O2 while waiting for transport
   Airway must be established
   IV antibiotic- ID pathogen
   PO antibiotics to follow
   Corticosteroids to reduce swelling
   Prevention with HIB at 2,4,6 or12, and 15 months

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